Conductance catheter-based assessment of arterial input impedance, arterial function, and ventricular-vascular interaction in mice
- 1 March 2005
- journal article
- research article
- Published by American Physiological Society in American Journal of Physiology-Heart and Circulatory Physiology
- Vol. 288 (3) , H1157-H1164
- https://doi.org/10.1152/ajpheart.00414.2004
Abstract
Global assessment of both cardiac and arterial function is important for a meaningful interpretation of pathophysiological changes in animal models of cardiovascular disease. We simultaneously acquired left ventricular (LV) and aortic pressure and LV volume (VLV) in 17 open-chest anesthetized mice (26.7 ± 3.2g) during steady-state (BL) and caval vein occlusion (VCO) using a 1.4-Fr dual-pressure conductance catheter and in a subgroup of eight animals during aortic occlusion (AOO). Aortic flow was obtained from numerical differentiation of VLV. AOO increased input impedance ( Zin) for the first two harmonics, increased characteristic impedance (0.025 ± 0.007 to 0.040 ± 0.011 mmHg·μl−1·s, P < 0.05), and shifted the minimum in Zin from the third to the sixth harmonic. For all conditions, the Zin could be well represented by a four-element windkessel model. The augmentation index increased from 116.7 ± 7.8% to 145.9 ± 19.5% ( P < 0.01) as well as estimated pulse-wave velocity (3.50 ± 0.94 to 5.95 ± 1.62 m/s, P < 0.05) and arterial elastance ( Ea, 4.46 ± 1.62 to 6.02 ± 1.43 mmHg/μl, P < 0.01). AOO altered the maximal slope ( Emax, 3.23 ± 1.02 to 5.53 ± 1.53 mmHg/μl, P < 0.05) and intercept (−19.9 ± 8.6 to 1.62 ± 13.51 μl, P < 0.01) of the end-systolic pressure-volume relation but not Ea/ Emax (1.44 ± 0.43 to 1.21 ± 0.37, not significant). We conclude that simultaneous acquisition of Zin and arterial function parameters in the mouse, based solely on conductance catheter measurements, is feasible. We obtained an anticipated response of Zin and arterial function parameters following VCO and AOO, demonstrating the sensitivity of the measuring technique to induced physiological alterations in murine hemodynamics.Keywords
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